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. 2022 Dec 25;12(1):39–48. doi: 10.1093/toxres/tfac079

The protective effect of red cabbage on water-soluble fractions of spent crankcase oil-induced alterations in lipid function biomarkers and atherogenic indices in male Albino rats

G E Bekibele 1,2,✉, F C Anacletus 3,4, K C Patrick-Iwuanyanwu 5,6, I L Nwaogazie 7
PMCID: PMC9972813  PMID: 36866218

Abstract

Spent crankcase oil (SCO) contains a cocktail of metals and polycyclic aromatic hydrocarbons (PAHs), transferred to the associated water-soluble fractions (WSF); and low-dose heavy metals exposures could increase the triglycerides (TG), total cholesterol (TC), low-density lipoproteins (LDL), and very-low-density lipoproteins (VLDL) concentrations. Hence, this study estimated the changes in the lipid profile and atherogenic indices (AI) of male Wistar albino rats exposed to the WSF of SCO and treated with aqueous extracts (AE) of red cabbage (RC) for 60 and 90 days. Sixty-four male Wistar rats divided into 8 groups (8 animals each) were orally administered 1 mL of deionized water, 500 mg/kg AE of RC, 1 mL of 25%, 50%, and 100% WSF of SCO daily for 60 and 90 days, whereas alternate groups were given the stated percentages of the WSF and the AE. Serum TG, TC, LDL, and VLDL concentrations were then analyzed using appropriate kits and the AI estimated thereafter. Although the 60 days study presented a nonsignificant (P < 0.05) difference in the TG, VLDL, and high density lipoprotein (HDL)-C levels in all the exposed and treated groups, a significantly (P < 0.05) elevated TC and non-HDL was recorded for the 100% exposed group alone. Also, the LDL concentration of all exposed groups was higher than all treated groups. The findings at the 90th day was different, such that the 100% and 25% exposed only groups had elevated lipid profile (except HDL-C) concentrations and AI compared with other groups. RC extracts can act as good hypolipidemic agents in WSF of SCO hyperlipidemia potentiating events.

Keywords: spent crankcase oil, red cabbage, lipid profile, atherogenic indices, male rats

Graphical Abstract

Graphical Abstract.

Graphical Abstract

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1. Introduction

At the root of the etiology of lipid metabolism related disorders which later progresses to cases of cardiovascular diseases (CD), as indicated by several studies are factors like: the shift from plant-based diets to the popular “Western diet,” genetic disorders, and specific drugs. However, more recently several findings have linked the impact of environmental toxicants like heavy metals,1–4 due to their ROS-induction capacity, known to exacerbate the breakdown of cellular membranes (from lipid peroxidation), and also alter important enzymatic functions. Heavy metal-induced ROS generation has also been shown to cause LDL-oxidation—an important factor in the early stages of atherosclerosis.5 Metals like cadmium are known to destroy channels for body fluids, obstruct endothelial function, while exacerbating atherosclerosis through ROS-generation processes.6 Lead on the other hand, has also been demonstrated to cause protein breakdown as well as lipid peroxidation.7 These metals are also able to mimic the biological activity of certain metals in the essential category (Fe, Zn, and Ca), by attaching to enzymes that would have otherwise needed the essential metals for their functionality, thereby hampering on their catalytic abilities.8 Spent crankcase oil (SCO), consists of a mixture of metals and polycyclic aromatic hydrocarbons imparted under ultra- temperature conditions and high mechanical stress,9 which could be passed on to the associated water-soluble fractions (WSF).10

Although synthetic drugs have been applied in treatment regimens, the subsequent side effects may not be too palatable, stressing the need for other naturally derived hypolipidemic agents. Red cabbage (RC) is an herbaceous biennial dicotyledonous plant, whose hypolipidemic effects have been widely studied.11–13 The vegetable’s rich supply of flavonoids and vitamins help prevent or control the incidence of ROS-related body disturbances that may culminate in CD, making it a good alternative candidate for the treatment of hypercholesterolemic and hypertriglyceridemic occurrences from environmental toxic exposures; as well as other sources. HPLC studies of the aqueous extracts (AE) suggests that the flavonoids isolated (including gallocatechin, epigallocatechin, and epicatechin), and the cinnamic acids (gallic, cinnamic and dicaffeoyl quinnic) may be responsible for the hypolipidemic effect witnessed.14

So far, studies bordering on SCO’s ability to cause dyslipidemia, or its amelioration are lacking, necessitating the present study under investigation. This study seeks to estimate the changes in the lipid profile and atherogenic indices (AI) of experimental animals on exposure to the water-soluble fractions of SCO, as well as RC’s ameliorative capacity in these exposures.

2. Methods

2.1. RC collection and identification

The RC used in this study was harvested from a local farm in Rayfield, Jos South Local Government Area of Plateau state, North Central, Nigeria in October 2020. At “the Herbarium Unit” of the Department of Plant Science and Biotechnology of the University of Port Harcourt, the plant was presented for identification. After which, documentation of the received samples was done and filed by assigning a reference number: UPH/PSB/2021/012, and a herbarium number: UPH/P/243 for later referencing purposes.

2.2. Red cabbage AE preparation

Freshly harvested RC leaves were washed under running water to remove dirt and other contaminants. When water droplets had been expunged, the vegetable was sliced and ground to a slurry to break the cell walls of the plant with the aid of a laboratory blender (Panasonic, MX-337N). Then 350 g of the slurry were measured out, to which ~300 mL of deionized water was added, after which the mixture was allowed to stand with frequent agitations in an adequately sealed beaker for 24 h. The extracts were then filtered out with the aid of a Whatman No. 1 filter paper and stored at 4 °C in a refrigerator for use. The extract was freshly prepared every 7 days, to maintain its freshness and preserve the phytochemicals present.

To estimate the dose to give to the test rats, a measured quantity of the extract was exposed to drying in an oven, after which the resulting extract was then weighed.

2.3. Collection of SCO

SCO was sourced from the car servicing ports of “God Is Good” multistate travelling agency in Port Harcourt City Local Government Area of Rivers State, Nigeria.

2.3.1. Preparation and preservation of the WSF

The WSF (a tentative reproduction of the groundwater model in the Niger Delta areas of South–South Nigeria) was prepared with slight modifications to the methods described by Anderson et al.,15 modified by Ogali et al.,10 and adopted by Patrick-Iwuanyanwu et al.,16 where a 1:8 oil to water mixture (putting the water beds in Rivers state into consideration), as an estimated concentration in ground water located in soils contaminated with SCO, was chosen by introducing 100 mL of oil to 700 mL of deionized water in a 1,000-mL equilibrating flask. The flasks were secured on a magnetic stirrer (Magnetic Stirrer hot plate 85-2, Lab Science, England) and agitated at 200 rpm for 24 h, after which time the flasks were allowed to equilibrate at room temperature for 6–12 h. The content was then poured into a separating flask, and the aqueous phase drawn off through a sidearm near the bottom of the flask into a 500-mL volumetric flask after a clear demarcation between the oil and water layers had been seen. The water layer was then stored in an amber colored Winchester bottle and kept in a refrigerator until use.

2.4. Animal handling

The 64 male Wistar albino rats, ~6 weeks old, also weighing between 130 and 150 g used in the study were obtained from the Animal House of the Department of Experimental Pharmacology and Toxicology, University of Port Harcourt, Choba, Rivers State, Nigeria. The animals were maintained in polypropylene cages under controlled conditions of temperature (23 ± 2 °C), 12 h light–dark cycle, and 50–60% relative humidity, where they were acclimatized for 7 days before the commencement of experiments. The normal rat chow and deionized water were provided ad libitum during the period. The experimental protocol was duly approved by the University of Port Harcourt Research Ethics Committee with UPH/CEREMAD/REC/MM72/085 assigned as the reference number.

2.5. Experimental design

The LC50 of WSF of SCO had been reported to be >100% concentration (Patrick-Iwuanyanwu et al.16). Three different exposures concentrations were chosen after making the water-soluble fraction, 100% (highest concentration consisting of the constituted water-soluble fraction without dilution with deionized water), 50% (medium concentration constituted by adding 50 mL of deionized water to 50 mL of the water-soluble fraction), and 25% (least concentration made by adding 75 mL of deionized water to 25 mL of the water-soluble fraction). Acute toxicity studies determined the LD50 of RC to be greater than 5,000 mg/kg.17 Hence 1/10 of the LD50, which is 500 mg/kg, was used as the dosage for the amelioration.

After the acclimatization period, subchronic and chronic studies were carried out on 64 male Wistar albino rats for 60 and 90 days. The rats were randomly divided into 8 groups, having a total of 4 animals in a group for the 60 and 90 days study. Volumes of extracts and toxicant were introduced orally once daily, 7 days in a week, as stated in Table 1.

Table 1.

Experimental design for ameliorative capacity of RC AE in the WSF of SCO exposed rats for 60 and 90 days.

Group 1 (8 rats) Group 2 (8 rats) Group 3 (8 rats) Group 4 (8 rats) Group 5 (8 rats) Group 6 (8 rats) Group 7 (8 rats) Group 8 (8 rats)
Control (deionized water and feed alone for 60 and 90 days) 500 mg/kg aqueous RC extract for 60&90 days 1 mL 100% WSF and feed alone for 60 and
90 days		 1 mL 50% WSF and feed alone for 60 and
90 days		 1 mL 25% WSF and feed alone for 60 and
90 days		 1 mL 100% WSF and 500 mg/kg extract for 60
and 90 days		 1 mL 50% WSF and 500 mg/kg extract for 60
and 90 days		 1 mL 25% WSF and 500 mg/kg extract for 60
and 90 days.
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2.6. Sample collection

At the 60th and 90th day of the experiment, morphologic abnormalities and other changes noticed in the rats in the course of experimentation were noted, and the rats anaesthetized in a diethyl ether-saturated chamber. After which, 4 mL of blood was drawn from the rats by a puncture to the heart, and put in plain sample bottles, and spun for the assays.

2.7. Body weight

The body weights of the test animals were taken weekly all through the experimental period using an ME303E weighing balance.

2.8. Lipid profile analysis

The triglycerides (TG), total cholesterol (TC) and high density lipoprotein (HDL) cholesterol were estimated by spectrophotometry using Fortress Diagnostics commercial kits, United Kingdom, with the concentration calculated using:

graphic file with name DmEquation1.gif (1)

where Inline graphic A stands for change in the absorbance of the sample and standard.

The low density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) cholesterol concentrations were estimated with the aid of the Friedwald, Levy, and Fredrickson18 equation, as represented below:

graphic file with name DmEquation2.gif (2)
graphic file with name DmEquation3.gif (3)

2.9. Calculation of AI

The non-HDL cholesterol concentration was calculated using the equation described by Brunzell et al.19

Non-HDL cholesterol = [Total cholesterol] – [HDL-C].

Other AI were estimated using the method adopted by Ikewuchi and Ikewuchi,20 as captured below:

graphic file with name DmEquation4.gif

 

graphic file with name DmEquation4a.gif

 

graphic file with name DmEquation4b.gif

2.10. Statistical analysis

The results from the experiment were analyzed using XLSTAT 2016 for windows and data represented as mean ± S.D. Total variations present in a set of data was estimated by 1-way analysis of variance (ANOVA), followed by Turkey’s test for multiple group comparisons. Statistical significance was set at P ≤ 0.05 in comparison with the control.

3. Results

3.1. Body weight

The body weight of male Wister albino rats exposed orally to 100%, 50%, and 25% WSF of SCO and the alternate treated groups with 500 mg/kg RC AE after 60 and 90 days is presented in Figs. 1 and 2.

Fig. 1.

Fig. 1

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Line graph showing mean body weight for male Wistar albino rats following oral exposure to WSF of SCO and RC AE for 60 days.

Fig. 2.

Fig. 2

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Line graph showing mean body weight for male Wistar albino rats following oral exposure to WSF of SCO and RC AE for 90 days.

The results show that there was no significant (P ≤ 0.05) difference in the average body weight of the animals in the 2 control groups and those exposed to 100%, 50%, and 25% WSF of SCO and the alternate treated groups with 500 mg/kg RC AE after 60 and 90 days exposure.

3.2. Lipid function biomarkers after 60 days exposure

Figures 3 and 4 are descriptions of the TG, CHOL, HDL, LDL, VLDL, and non-HDL concentrations of male Wister albino rats following oral exposure to the WSF of SCO and RC AE for 60 days.

Fig. 3.

Fig. 3

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Multiple bar graphs showing mean concentrations of Trig, Chol, and LDL in male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 60 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

Fig. 4.

Fig. 4

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Multiple bar graphs showing mean concentrations of HDL, VLDL, and Non-HDL in male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 60 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

From the result of the analysis, there was no significant (P ≤ 0.05) difference in the TG and VLDL concentration of the WSF of SCO exposed groups and the alternate WSF of SCO treated groups compared with the untreated control and 500 mg/kg RC AE group. Likewise, the cholesterol and non-HDL analysis revealed that while the 100% WSF of SCO group was significantly (P ≤ 0.05) higher than the untreated control, as well as other exposure and treatment groups, there was no significant (P ≤ 0.05) difference between the other groups and the untreated control. Also, the HDL concentration for the 100% WSF of SCO group was nonsignificantly (P ≤ 0.05) lower than the untreated control, as well as other exposure and treatment groups, whereas that of other groups recorded a nonsignificant (P≤ 0.05) difference compared with the untreated control. However, a change in trend was seen in the LDL concentration as a significant (P ≤ 0.05) rise was recorded for the 500 mg/kg RC AE group, 100% WSF of SCO, 50% WSF of SCO, 25% WSF of SCO and the alternate RC extracts treated groups compared with the untreated control. Intergroup comparison shows that the 100%, 50%, and 25% WSF of SCO groups had a significantly (P ≤ 0.05) increased LDL concentration compared with the alternate treated groups.

3.3. Lipid function biomarkers after 90 days exposure

Figure 5 and 6 are descriptions of the TG, CHOL, HDL, LDL, VLDL, and non-HDL concentrations of male Wistar albino rats following oral exposure to the WSF of SCO and RC AE after 90 days.

Fig. 5.

Fig. 5

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Multiple bar graphs showing mean concentrations of Trig, Chol, and LDL in male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 90 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

Fig. 6.

Fig. 6

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Multiple bar graphs showing mean concentrations of HDL, VLDL, and Non-HDL in male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 90 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

A significant (P ≤ 0.05) increase in the TG and VLDL concentrations of the 500 mg/kg RC AE group, WSF of SCO exposed groups and the alternate WSF of SCO treated groups (the 25% WSF of SCO RC treated group was an exception as there was no significant difference with the control) was recorded compared with the untreated control. Similarly, the cholesterol and Non-HDL concentrations of the WSF of SCO exposed groups and the alternate WSF of SCO treated groups (except the 25% WSF of SCO RC treated group which was not significantly different from the control) was significantly (P ≤ 0.05) elevated compared with the untreated control and the 500 mg/kg RC AE group. Comparison within exposed and treated groups shows that the 100% and 25% WSF of SCO groups had a significantly increased CHOL concentration compared with the alternate treated groups, whereas a nonsignificant difference was recorded for the 50% WSF of SCO exposed and treated groups. Contrary to the findings for other parameters, there was no significant difference in the HDL concentration for the 500 mg/kg RC AE group, WSF of SCO exposed groups and the alternate WSF of SCO treated groups in comparison with the untreated control. A close similarity in the LDL concentration of the 60 days study was recorded in the 90 days study where a significant rise was recorded for the 100% WSF of SCO, 25% WSF of SCO and the alternate RC extracts treated groups (except the 25% WSF of SCO RC treated group which was not significantly different from the control), compared with the untreated control. On the other hand, the LDL concentration for the 50% WSF of SCO was not significantly different from the untreated control.

3.4. Atherogenic indices of male Wistar albino rats

Fig. 7 is a presentation of the Cardiac risk ratio (C.R.R.), atherogenic coefficient (AC), and atherogenic index (AI) of male Wistar albino rats following oral exposure to the WSF of SCO and RC AE after 60 days.

Fig. 7.

Fig. 7

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Multiple bar graphs showing mean values of C.R.R., A.C., and A.I. of male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 60 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

From the estimations, there was no significant (P ≤ 0.05) difference in the C.R.R. of the WSF of SCO exposed groups and the alternate WSF of SCO treated groups compared with the untreated control and the group that received the 500 mg/kg RC AE. Intergroup analysis also revealed that there was no significant (P ≤ 0.05) difference between the exposed and the treated groups. The AC and AI estimates were significantly (P ≤ 0.05) increased for the 100% WSF of SCO exposed group compared with the untreated control and the other groups. Similarly, intergroup analysis revealed that there was no significant difference between the 50% and the 25% WSF of SCO exposed and the treated groups, whereas a significant (P ≤ 0.05) increase in the 100% WSF of SCO exposed group compared with the treated group was recorded.

3.5. Atherogenic indices of male Wistar albino rats

Figure 8 shows the Cardiac risk ratio (C.R.R.), AC, and AI of male Wistar albino rats following oral exposure to the WSF of SCO and RC AE after 90 days. The C.R.R. result demonstrated significant (P ≤ 0.05) increases in the 100%, and 25% WSF of SCO exposed groups compared with the control. The AC calculations showed that the 100%, and 25% WSF of SCO exposed groups and the 100% treated group significantly (P ≤ 0.05) increased compared with the control and the 500-mg/kg RC AE group. As in the C.R.R. estimates, the AI calculations revealed significant (P ≤ 0.05) increases in the 100%, and 25% WSF of SCO exposed groups compared with the control. As stated in the estimations above, comparison within exposed and treated groups showed that the 100% and 25% WSF of SCO groups had a significantly increased C.R.R. compared with the alternate treated groups, whereas a nonsignificant difference was recorded for the 50% WSF of SCO exposed and treated groups.

Fig. 8.

Fig. 8

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Multiple bar graphs showing mean values of C.R.R, A.C., and A.I. of male Wistar albino rats, following oral exposure to the WSF of SCO and AE of RC for 90 days. Different alphabets indicate significant difference (P ≤ 0.05) between groups.

4. Discussion

Body weight is the force exerted as a consequence of gravity’s effect on body mass represented in Newton. Toxic compounds have been shown to either bring about an elevation or reduction in body weight.21 Several studies conducted to determine the toxic endpoints emanating from SCO exposures have documented a marked decrease in the body weight of test animals compared with the control animals.22–25 These were however, contrary to the findings of this research, where body weight changes among the exposure groups were not significantly different from the groups treated with RC and the controls in the 60 and 90 days study periods, which may have been as a result of the ratio of oil to water used in this study, which made it less toxic. The nonsignificant difference in the weight of rats exposed to drinking water tainted with SCO findings in the study by Ochiogu et al.,26 were in agreement with the results of this work.

The results after the 60 days exposure to the WSF of SCO presented an onset of hypercholesterolemia with a significant reduction in the HDL level in the group that received 100% WSF of SCO alone, while the lipid profile of other groups were not significantly different from the control. The 90 days study differed from the above, such that the existence of hypertriglyceridemia, hypercholesterolemia, and hyperlipoproteinemia were reported in all the exposed groups. However, a significant reduction of these values were seen in the 100% and 25% groups that received the RC, proof that RC may have hypolipidemic effect against the WSF of SCO induced dyslipidemia. The incidence of hyperlipoproteinemia and a corresponding reduction in HDL levels may be indicative of the onset of atherosclerosis on exposure to the WSF of SCO. Existing studies have shown that a high TG, CHOL, LDL, and VLDL levels coupled with low HDL levels portends significant predisposition to cardiovascular diseases (CD).2,27,28 This is because, increased LDL cholesterol could translate to increased oxidation and absorption through arterial walls, tending towards elevated binding to arterial proteoglycans trapping them in the arterial wall; and the formation of artherosclerotic plaques further causes CD progression in cases of myocardial infarction or ischemic heart disease.29 The dyslipidemia noticed in these exposures may have occurred as a result of serious alterations in lipid metabolism possibly arising from an inhibition of certain enzymatic activities; such as lipoprotein lipase responsible for the breakdown of TG. It has been indicated that elevated TG, TC, VLDL, LDL, non-HDL levels followed by a low HDL concentration are characteristic of heavy metal exposure studies.30 Anyanwu et al.,2 also attested to the impact of low-dose heavy metals exposures on the lipid profile of experimental animals; indicating a noticeable spike in TC, TG, LDL, and VLDL levels, and a corresponding decrease in HDL levels. These effects appeared to have been reversed on exposure to Costus afer AE. In a recent article,1 correlations were made linking Cd, Pb, Hg, and As exposures to alterations of lipid metabolic pathways (mostly caused by altered genes), specifically hampering β-oxidation, lipid endogenous metabolic pathways, FFAs (free fatty acids), TG, cholesterol (CHOL), and phospholipids production and transport. In the same way, inhaling benzo(a)pyrene caused alterations in lipid metabolism, attacking glycerol-phospholipids specifically.31

Several studies have looked into the beneficial effects of anthocyanin; a member of the flavonoid class, in CD states. The anti-dyslipidemia effect from RC treatments has been captured by many studies11–13; where a reduction in TG, CHOL and LDL-C were recorded. However, as noted in these studies and in the present study, the extracts did not bring about an increase in HDL-C. The CD-reduction ability of anthocyanin could be a function of the elevated serum antioxidant capacity when consumed, which consequently forestalls LDL-C oxidation, a first step in atherosclerotic events.32

Atherogenic indices are useful pointers to the prevalence of atherosclerotic and cardiovascular disease risks associated with the serum lipid levels assayed in the samples.33 The atherogenic index (AI) is an important marker of atherogenicity, whereas cardiac risk ratio is a potent indicator of CD risk. Also, in the event of an absent Apo lipoprotein B measured level, AC (which is a ratio of non-HDL to HDL levels), provides adequate information on a rising CD risk from various exposures. Findings from the study under consideration were in agreement with those of Igharo et al.3; where AC and C.R.R. values of heavy metals exposed groups were higher than control groups. The results from the study show that continuous exposure to the water-soluble fractions of SCO at elevated concentrations could increase the risk of developing cardiovascular related diseases over extended periods.

5. Conclusion

This work has presented alterations in the lipid profile of rats brought about by oral exposure to the water-soluble fractions of SCO over extended periods, which were significantly reversed on treatment with RC. It also proves that such continuous exposures could further predispose one to cardiovascular risks, which can be averted when diets rich in vegetables are consumed daily.

Authors’ contributions

All authors made contributions to the study conception and design. Material preparation, data collection and analysis were performed by Bekibele Grace Eserophe, Anacletus C. Francis, Patrick-Iwuanyanwu C. Kingsley, and L. Ify Nwaogazie. The manuscript’s first draft was compiled by Bekibele Grace Eserophe, and all authors edited previous versions of the manuscript. All authors read and approved the final manuscript.

Funding

This work received part funding from the World Bank Africa Centre of Excellence in Public Health and Toxicological Research, University of Port Harcourt, Rivers State, Nigeria.

Conflict of interest statement. The authors declare that there are no conflicting interests.

Data Set Reference

Bekibele GE, Anacletus FC, Patrick-Iwuanyanwu KC, Nwaogazie IL. 2022 Data Set for The Protective Effect of Red Cabbage on Water-Soluble Fractions of Spent Crankcase Oil-Induced Alterations in Lipid Function Biomarkers and Atherogenic Indices in Male Albino Rats. http://doi.org/10.6084/m9.figshare.20391660.

Contributor Information

G E Bekibele, Africa Centre of Excellence in Public Health and Toxicological Research, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria; Department of Biochemistry, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria.

F C Anacletus, Africa Centre of Excellence in Public Health and Toxicological Research, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria; Department of Biochemistry, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria.

K C Patrick-Iwuanyanwu, Africa Centre of Excellence in Public Health and Toxicological Research, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria; Department of Biochemistry, University of Port Harcourt, P.M.B. 5323, Choba 500004, Rivers State, Nigeria.

I L Nwaogazie, African Centre of Excellence for Oilfield Chemicals Research (ACE-CEFOR), University of Port Harcourt, Port Harcourt, Choba 500004, Nigeria.

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